Evidence map›Paper›PMID 38178583›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

BRCC36 Deubiquitinates HMGCR to Regulate the Interplay Between Ferroptosis and Pyroptosis.

Haiyan Wang, Long Shu, Cairui Lv, Na Liu, Yao Long, Xintong Peng, Huli Ling, Tania Tao, Jun Tang, Yan Cheng and 3 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
13.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 33 citations in OpenAlex.

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  14. Combinatorial chemistry & high throughput screening · 2026
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  20. Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 1 institution in 3 countries.

Haiyan WangKey Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078, China.
Long ShuKey Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078, China.
Cairui LvKey Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078, China.
Na LiuKey Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078, China.
Yao LongKey Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078, China.
Xintong PengKey Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078, China.
Huli LingKey Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078, China.
Tania TaoKey Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078, China.
Jun TangKey Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078, China.
Yan ChengDepartment of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha, 410011, China.
Shuang LiuDepartment of Oncology, Institute of Medical Sciences, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Desheng XiaoDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Yongguang TaoKey Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078, China.ORCID 0000-0003-2354-5321
Central South University · CN

Funding

Central South University Research Program of Advanced Interdisciplinary Studies 2023QYJC030Hunan Provincial Key Area R&D Programs 2021SK2013National Natural Science Foundation of China 81772927National Natural Science Foundation of China 81872285National Natural Science Foundation of China 81874139National Natural Science Foundation of China 82072594National Natural Science Foundation of China 82073097National Natural Science Foundation of China 82272982National Natural Science Foundation of China 8237112964Natural Science Foundation of Hunan ProvinceScience and Technology Innovative Research Team in Higher Educational Institutions of Hunan Province 2022RC3072
6 · The paper itself

Abstract

Various forms of programmed cell death (PCD) exhibit distinct characteristics depending on their specific molecular mechanisms, and there are interactions among these different forms. Ferroptosis, which is related to autophagy and apoptosis, has an unknown potential interaction with pyroptosis. This study revealed a mutually antagonistic relationship between ferroptosis and pyroptosis, with 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) playing a key role in their interaction. It is found that HMGCR predominantly localized to mitochondria during ferroptosis but shifted to the endoplasmic reticulum following treatment with a pyroptosis inducer. Furthermore, this study demonstrated that BRCC36 (BRCA1/BRCA2-containing complex subunit 36) deubiquitinated HMGCR in a manner dependent on deubiquitinating enzyme (DUB) activity, and inhibited ferroptosis and promoted pyroptosis. Moreover, as an oncogene in hepatocellular carcinoma (HCC), BRCC36 promoted cancer cell proliferation, migration, invasion, and tumor growth. Thiolutin, an inhibitor of BRCC36, effectively suppressed the interaction between BRCC36 and HMGCR, leading to the inhibition of HCC growth. Therefore, targeting BRCC36 can offer a novel and promising therapeutic strategy for HCC treatment. In conclusion, these findings provide new theoretical evidence for further characterizing tumor heterogeneity and offer new molecular targets for the diagnosis and treatment of HCC.

Indexed as

Carcinoma, HepatocellularFerroptosisLiver NeoplasmsHumansHydroxymethylglutaryl CoA ReductasesOxidoreductasesPyroptosisHMGCR protein, humanHydroxymethylglutaryl CoA ReductasesOxidoreductasesBRCC36endoplasmic reticulumferroptosisHMGCRmitochondriapyroptosis

Identifiers

PMID38178583
PMCPMC10953584
OpenAlexW4390612197

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.